Pharmaceutical Prodrug

By: Pharma Tips | Views: 13287 | Date: 18-Jun-2010

A prodrug is a pharmacological substance (drug) that is administered in an inactive (or significantly less active) form. Once administered, the prodrug is metabolised in vivo into an active metabolite. The rationale behind the use of a prodrug is generally for absorption, distribution, metabolism, and excretion (ADME) optimization.

A prodrug is a pharmacological substance (drug) that is administered in an inactive (or significantly less active) form. Once administered, the prodrug is metabolised in vivo into an active metabolite. The rationale behind the use of a prodrug is generally for absorption, distribution, metabolism, and excretion (ADME) optimization. Prodrugs are usually designed to improve oral bioavailability, with poor absorption from the gastrointestinal tract usually being the limiting factor.
Additionally, the use of a prodrug strategy increases the selectivity of the drug for its intended target. An example of this can be seen in many chemotherapy treatments, in which the reduction of adverse effects is always of paramount importance. Drugs used to target hypoxic cancer cells, through the use of redox-activation, utilise the large quantities of reductase enzyme present in the hypoxic cell to convert the drug into its cytotoxic form, essentially activating it. As the prodrug has low cytotoxicity prior to this activation, there is a markedly lower chance of it "attacking" healthy, non-cancerous cells which reduces the side-effects associated with these chemotherapeutic agents.
In rational drug design, the knowledge of chemical properties likely to improve absorption and the major metabolic pathways in the body allows the modification of the structure of new chemical entities for improved bioavailability. Sometimes the use of a prodrug is unintentional, however, especially in the case of serendipitous drug discoveries, and the drug is only identified as a prodrug after extensive drug metabolism studies

Pharmaceutical Prodrug
Table 1: Classification of prodrugs
Type Converting site Subtype Tissue location of conversion Examples
Type I Intracellular Type IA Therapeutic target tissues/cells Zidovudine, 5-Flurouracil
Type I Intracellular Type IB Metabolic tissues (liver/lung etc) Captopril, Cyclophosphamide
Type II Extracellular Type IIA GI fluid Sulfasalazine, Loperamide oxide
Type II Extracellular Type IIB Systemic circulation Fosphenytoin, Bambuterol
A prodrug can belong to both a Type IA and IB category when the site of the therapeutic target and conversion are the same (e.g., HMG Co-A reductase inhibitors).
Valacyclovir is converted by esterase to the active acyclovir 
Levodopa is converted by DOPA decarboxylase to the active dopamine 
Chloramphenicol succinate ester is used as intravenous prodrug of chloramphenicol, because pure chloramphenicol does not dissolve in water 

 For a drug, most often an Organic chemical, to elicit a pharmacological response must reach a "site of action". 
 The term site of action appears frequently in the scientific/ medical literature and refers to the fact that a chemical must reach and interact with receptor in some host target site in order to act as a therapeutic agent.
 There are barrier that might limit the ability of a drug to reach its" site of action ". These barriers lead to formation of a new phenomenon called " prod rug"
 Basically prodrug is a pharmacologically inactive compound that is transformed by mammalian system into active substance by either chemical or by metabolic means .
 This include both compounds that are designed to undergo a transformation in order to yield an active substance and those that were discovered by serendipity to do so.
 A prodrug is a chemically modified inert drug precursor, which upon biotransformation
  liberates the pharmacologically active parent compound
 Conversation in active forms accomplished by enzymes 
  A prodrug is also called drug latentiation
 Ideally, conversion occurs as soon as the desired goal for Designing the prodrug is achieved
 Prodrugs and soft drugs are opposite Almost all drugs posses some undesirable physiochemical and biological properties.
 Minimizing or eliminating the undesirable properties oan improve their therapeutic efficacy. 

It can be achieved by three approaches. 

1. Biological approach:To alter the route of administration, which mayor may not    be accepted by patients
2. Physical approach:Modify the design of the dosage form such as controlled delivery of drugs. 
3 chemical approaches: By enhancing drug selectivity while minimizing drug toxicity. 

There are three chemical approaches: 

 Design have hard and soft drugs. 
 Design and development of new drugs with desirable Features. 
 Design of pro drugs

Ideal Drug Carriers 

 Protect the drug until it reaches the site of action .
 Localize the drug at the site of action 
 Minimize host toxicity 
 Are biodegradable, inert, and nonimmunogenic 
 Are easily prepared and inexpensive 
 Are stable in the dosage form


 Harper (1959) has elaborated this concept by defining the term "DRUG LATEN1IATION" as the chemical modifications of a biologically activity compound to form a new chemical entity, the prodrug. 
 . Wermuth (1944) divided the prodrug into two classes. 

 Hard drug: - 
It is non- metabolically compound having. high lipid solubility or high water solubility having long biological half-life 
Exam. Cocaine and heroin. 

 Soft drug: - 
It is biologically active compound that is biotransformed in vivo in a rapid and predictable manner in to non toxic moieties 
Exam. Insulin and adrenaline. 

 Carrier linked prodrugs :-
Which result from a temporary linkage of the active drug molecule with a carrier group of promoiety.

 Bioprecursors:-
Which result from a molecular modification of the active compound itself. This modification generates a new compound, which acts as a substrates for the metabolizing enzymes, and metabolite being the expected active agent

 Mutual prodrug:-
Prodrug comprises of two pharmacologically active agents coupled together to form a single molecules such that each act as the carrier for the other.Such prodrug of two active compounds are called as mutual prodrug
 A compound that contains an active drug linked to a carrier group that is removed enzymatically 
 They are generally esters or amides such a prodrug have greatly modified lipohilicity due to the atteched carrier. 
 The active drug is realised by hydrolytic cleavage, either chamicaliy or enzymically 
  In carrier linked prodrug, a drug molecule, the usefulness of which is limited by its adverse physicochemical properties is attached to a carrier groups of promoiety to form a new compound i.e prodrug . from which the pattern drug is regenerated in prodrug can be considered as drug contating specialized nontoxic protective group utilized in a transient manner to alter or eliminate the undesirable properties of the parent drug molecule. 
 Formation of prodrug does not alter the primary structure of the parent drug and the unique failure of this approach is that the physicochemical properties can be tailored by means of changing the structure of promoiety and intrinsic activity of the parent drug is. assured through the in vivo cleavage of the prodrugs. 
 A well - designed prodrug should satisfy the following criteria Linkage between drug molecule and carrier group is usually a covalent bond. 
  The prodrug should be biologically inactive. 
 Chemical linkage between parent drug and promoiety must be bioreversible.prodrug should be sufficiently stable to allow its formulation into an appropriate dosage form. 
 Most common activation reaction is hydrolysis. 
 The cascade prodrug is a prod rug for which the cleavage of the Carrier group becomes effactive only after the unmasking an active Group 
 Double Prodrug or pro-prodrug -The double prodrug is a biologicaly 
 inactive molecule which is transformed invivo in two steps(enzymaticallyor chemically) to the active species. 

Carrier linked prodrug subdivided into 
A. bipartate 
 comprised of one carrier attached to drug 
B tripartite prodrug
 carrier connected to a linker that is connected to drugs. 

 The structure of most prodnigs are bipartate in nature, in which the parent drug is attached to directly to promoiety. However in certain cases this basic prodrug approach may _ fail to confer the desired properties to prod rug formed . 
 It is possible for example that bipartate prodrug may be unstable due to the inherent nature of drug- Promoiety bond. 
 Alternatively, the prodrug may be quite molecule may hinder "the cleavage of the prodrug to release the parent drug in vivo. These problems may be overcome by disigning tripartite prodrugs. utilizing a spacer or connector group between drug molecule and promoiety . 
 In this case drug molecule is pIa sed away from promoiety so that enzymatic activation now involves the cleavage of the spacer-group must be designed in such a way so that the- initial activation is followed by spontaneous cleavage of the remaining drug spacer bond under physiological conditions to release the parent drug. the strategy of using a spacer between drug and pro moiety has recently been suggested (carl et AI, 1981) and a model tripartite prodrug. 
 This tr iparate prodrug is quite stable in aqueous buffer in the absence of trypsin but in presence of trypsin undergoes rapid cleavage to release the parent - p - nitroaniline. 

 two, usually synergistic, drugs attached to each other 
 A bipartate or tripartite prodrug in which the carrier is a synergistic drug with the drug to which it is linked. 

o Ideal Mutual Prodrugs:-- 

 Well absorbed 
 Both components are released together and quantitatively after 
 Maximal effect of the combination of the two drugs occurs at 1: 1 ratio distribution/ elimination of components are similar antibacterial ampicillin ~-lactamase inactivatorpenicillanic acid sulfone. 

Hydrolysis gives 1: 1: 1 ampicillin : penicillanic acid sulfone 

 bioprecursor are inert rnolecules obtained by chemical modification of the active drug but do not contain a carrier. 
 such a moiety has almost the same lipophilicity as the parent drug and is bioactivated generally by redox  biotransformation, only enzymetically 
 Ex. Arylacetic acid NSAID such as fenbufen from aroyl propionic acid precursors. 


(a) Enzymatic Reversal 
 The conversion of prodrug to corresponding drug depend on presence of enzyme capable of metabolizing the promoiety drug linkage. Enzymes may be located in specific region within the body. 
 In which case their activity can be used in site-specific delivary of drugs. In many case however enzymes are ubiquitous, providing more  limited prodrug application. 
 wide interpatient variability may be accepted unless enzyme is present in excess 9i.e. esterases 
 In spite of this drawback enzymatic reversal of prodrugs has found for greater application than chemical reversal approach. 

(b) Chemical Reversal 
 The conversions of prodrug to corresponding drug depend on presence of chemical between the drug and promoiety. 
  The most common chemical reversal takes advantage of differential 16 hydrolysis arising from deference in pH in body e.g. the pH of stomach is lA, pH of intestine 5-8, blood pH is 7.4. 
  These differences have been utilized to design prodrug with increased gastric stability followed by reversal in intestine or blood other e.g. includesdry increase stability followed by chemical reversal in water for injection and prolongation of drug action through controlled prodrug hydrolysis in blood. 


 Improvement of taste 
 Improvement of odor 
 Change of physical form for preparation of solid dosage forms (4) Reduction of GI    irritation 
 Reduction of pain on injection 
 Enhancement of drug solubility and dissolution rate (hydrophilicity of drug) 
 Enhancement of chemical stability of drug 

 Enhancement of bioavailability (lipophilicity) 
 Prevention of presystemic metabolism 
 Prolongation of duration of action 
 Reduction of toxicity 
 site-specific drug delivery (drug targeting)

I. Improvement of taste 
 One of the reasons for poor patient compliance particulaly in case of children, is the bitterness, acidity or causticity of the drug. 
Two approaches can be 'utilized to overcome the bad taste of drug. 
is reduction of drug solubility in saliva and is to lower the affinity of 
drug towards taste receptors.  
Parent drug                                                    prodrug 
Chloramphenicol                                       Palmitate ester 
Prod rug to Increase Patient Acceptance 
The antibacterial drug clindamycin is bitter and not well tolerated by children.
Clindamycin palmitate is not bitter. 
clindomycin (R = H) 
clindomycin phosphate (R = P03H2) clindomycin palmitate (R = O{CH2) 14CH3) 
Either not soluble in saliva or does not bind to the bitter taste receptor or both

2. Improvement of odor 
The odor of a compound depends upon its vapor pressure >- A liquid with high vapor pressure will have strong odor 
e .g; Ethyl mercaptan which is a foul smelling liquid, 
it useful in the treatment of leprosy, is converted in to its pht.halate ester ,which has higher b.p. and odorless

3. Reduction of pain on injection 
 Intramuscular injection are particularly painful when the drug precipitates or penetrates into the surrounding cells or when the solution is strongly acidic, alkaline or alcoholic, E.g. the low aqueous solubility of clindamycin Hcl , the alkaline solution of  phenytoin are responsible for pain on injection. 
 This can be overcome by use of more water soIu bIe prodrugs of such agents. E.g. 2-phosphate ester of c1indamycin 

4. Prodrug to Eliminate Formulation Problems 
 Formaldehyde is a gas with a pungent odor that is used as a disinfectant. Too toxic for direct use.
 It is a stable solid that decomposes in aqueous acid . 
 The pH of urine in the bladder is about 4.8, so methenamine is used as a urinary tract antiseptic. 
 Has to be enteric coated to prevent hydrolysis in the stomach.

5.Prodrug for Improved Absorption Through Skin
corticosteroids - inflammation, allergic, pruritic skin conditions fluocinolone acetonide (R = H) 
fluocinonide (R = COCH3) 
Better absorption into cornea for the treatment of glaucoma
The cornea has significant esterase activity

6.Prodrug for Increased Water Solubility
 Choice of water solubilizing group: 
 The ester must be stable enough in water for a shelf life of > 2 years (13 year half-life),but must be hydrolyzed in vivo with a half-life < 10 minutes. Therefore, in vivo/in vitro lability ratio about 106. 
 To avoid formulation of etoposide with detergent,PEG, and EtOH (used to increase water solubility),it has been converted .to the phosphate prodrug

Areas of Improvem.ent for Prodrugs 
1.  site specificity 
2. protection of drug from biodegradation ?
3. minimization of side effects 
4. Site -specific drug delivery 
 After its absorption into systemic circulation the drug is distributed to the various parts of the. body including the target site as well as the nontarget tissues such a distribution pattern has several

Disadvantages :-- 
  Lead to undesirable toxic effects in non target tissues » A smaller fraction of the drug will reach its target site 
 If the target site has a long distribution time, the drug may get eliminated without reaching a site 
 Drug reaches the target cells in sufficient amounts, it may not .be able to penetrate into them. 
 Over come this problems by altering its disposition characteristics. 
 The prodrug converted into its active form only in the target organ or tissue by utilizing either specific enzymes or PH value different from the normal PH for activation

Example of selective uptake system 
 » mesalamine is a useful in treatment of ulcerative colitis. 
 It is not absorbed into the systemic circulation. 
 However following Oral administration, the drug is inactivated before reaching the lower intestine, the site of action. covalent binding of this agent to sulfaphridine yields the prodrug sulfasalazine, an azo compound. 
 » This prodrug reaches the colon intact where cleavage by the bacterial enzyme azo reductase releases the active mesalamine for local actio

5.  Prodrug Therapies
For selective activation of prodrugs in tumor cells Two steps

I. incorporate a prodrug-activating enzyme into a target tumor cell 
II. administer a nontoxic prodrug which is a substrate for the exogenous enzyme incorporated

Criteria for Success with Enzyme-Prodrug Therapies 

I. The prod rug-activating enzyme is either nonhuman or a human protein expressed poorly 
II. The prodrug-activating enzyme must have high catalytic activity 
III. The prodrug must be a good substrate for the incorporated enzyme and not for other endogenous enzymes 
IV. The prod rug must be able to cross tumor cell membranes 
V. The prodrug should have low cytotoxicity and the drug high cytotoxicity 
VI. The activated. drug should be highly diffusable to kill neighboring nonexpressing cells (bystander killing effect) 
VII. The half-life of the active drug is long enough for bystander killing effect but short enough to avoid leaking out of tumor cells 

(a) Antibody Directed Enzyme Prodrug Therapy (ADEPT) 

An approach for site-specific delivery of cancer drugs. 

l. Phase One: 
An antibody-enzyme conjugate is administered which binds to the surface of the tumor cells.The antibody used has been targeted for the particular tumor cell. 
The enzyme chosen for the conjugate is one that will be used to cleave the carrier group off of the prod rug administered in the next phase. 

2 .Phase Two: 
After the .antibody-enzyme has accumulated on the tumor cell and the excess conjugate is cleared from the blood and normal tissues, the prodrug is administered. 
The enzyme conjugated with the antibody at the tumor eel surface catalyzes the conversion of the prod rug to the drug when it reaches the tumor cell.

 Increased selectivity for targeted cell 
 Each enzyme molecule converts many prodrug Molecules 
 The released drug is at the site of action 
 Demonstrated to be effective at the clinical level 
 Concentrates the drug at the site of action 

1. Immunogenicity and rejection of antibody-enzyme. conjugate 
2. Complexity of the two-phase system and i.v.administration 
3. Potential for leakback of the active drug

(b) Antibody-Directed Abzyme Prodrug Therapy (ADAPT) 
  Instead of using a prod rug-activating enzyme, a humanized prodrug¬activating catalytic antibody (abzyrne) can be used. 
 Ideally, the abzyme catalyzes a reaction not known to occur In humans, so the only site where the prod rug could be activated is at the tumor cell where the abzyme is bound. 
 Antibody 38C2 catalyzes sequential retro-aldol and re tro-Mich ael reactions not catalyzed by any knownsss human enzyme. 
  Found to be long-lived in vivo, to activate prodrugs selectively, and to kill colon and prostate cancer cells. 

(c) Gene-Directed Enzyme Prodrug Therapy (GDEPT) 
 A gene encoding the prodrug-activating enzyme is expressed in target cancer cells under the control of tumor-selective promoters or by viral transfection. 
 These cells activate the prodru~ as in DEPT

Biggest problems in prodrug design is the toxicity which may be due to 

 Formation of an unexpected metabolite form the total prodrug that may be toxic. 
 The inert carrier generated following cleavage of prodrug may also transformed in to a toxic metabolite. 
 During its activation stage , the prodrug might consume a vital cell constituent such as glutathaione leading to its depletion.

Pro-drug approach in Antiviral Therapy

Introduction to Anti-viral Therapy:-
Antiviral drugs are a class of medication used specifically for treating viral infections. Like antibiotics for bacteria, specific antivirals are used for specific viruses. Antiviral drugs are one class of antimicrobials, a larger group which also includes antibiotic, antifungal and antiparasitic drugs. They are relatively harmless to the host, and therefore can be used to treat infections. They should be distinguished from viricides, which actively destroy virus particles outside the body.
Most of the antivirals now available are designed to help deal with HIV, herpes viruses (best known for causing cold sores and genital herpes, but actually causing a wide range of diseases), the hepatitis B and C viruses, which can cause liver cancer, and influenza A and B viruses. Researchers are now working to extend the range of antivirals to other families of pathogens.
Designing safe and effective antiviral drugs is difficult, because viruses use the host's cells to replicate. This makes it difficult to find targets for the drug that would interfere with the virus without harming the host organism's cells.
The emergence of antivirals is the product of a greatly expanded knowledge of the genetic and molecular function of organisms, allowing biomedical researchers to understand the structure and function of viruses, major advances in the techniques for finding new drugs, and the intense pressure placed on the medical profession to deal with the human immunodeficiency virus (HIV), the cause of the deadly acquired immunodeficiency syndrome (AIDS) pandemic.
Almost all anti-microbials, including anti-virals, are subject to drug resistance as the pathogens evolve to survive exposure to the treatment.
Viruses consist of a genome and sometimes a few enzymes stored in a capsule made of protein (called a capsid), and sometimes covered with a lipid layer (sometimes called an 'envelope'). Viruses cannot reproduce on their own, so they propagate by subjugating a host cell to produce copies of themselves, thus producing the next generation.
Researchers working on such "rational drug design" strategies for developing antivirals have tried to attack viruses at every stage of their life cycles. Viral life cycles vary in their precise details depending on the species of virus, but they all share a general pattern:
• Attachment to a host cell. 
• Release of viral genes and possibly enzymes into the host cell. 
• Replication of viral components using host-cell machinery. 
• Assembly of viral components into complete viral particles. 
• Release of viral particles to infect new host cells. 
(A) Anti-herpes virus :
(B) anti-influenza virus :
(B) Anti-

Anti-viral targeting technique
The general idea behind modern antiviral drug design is to identify viral proteins, or parts of proteins, that can be disabled. These "targets" should generally be as unlike any proteins or parts of proteins in humans as possible, to reduce the likelihood of side effects. The targets should also be common across many strains of a virus, or even among different species of virus in the same family, so a single drug will have broad effectiveness. For example, a researcher might target a critical enzyme synthesized by the virus, but not the patient, that is common across strains, and see what can be done to interfere with its operation.
Once targets are identified, candidate drugs can be selected, either from drugs already known to have appropriate effects, or by actually designing the candidate at the molecular level with a computer-aided design program.
The target proteins can be manufactured in the lab for testing with candidate treatments by inserting the gene that synthesizes the target protein into bacteria or other kinds of cells. The cells are then cultured for mass production of the protein, which can then be exposed to various treatment candidates and evaluated with "rapid screening" technologies.
Approaches by life cycle stage
Before cell entry
One anti-viral strategy is to interfere with the ability of a virus to infiltrate a target cell. The virus must go through a sequence of steps to do this, beginning with binding to a specific "receptor" molecule on the surface of the host cell and ending with the virus "uncoating" inside the cell and releasing its contents. Viruses that have a lipid envelope must also fuse their envelope with the target cell, or with a vesicle that transports them into the cell, before they can uncoat.
This stage of viral replication can be inhibited in two ways: 1. Using agents which mimic the virus-associated protein (VAP) and bind to the cellular receptors. This may include VAP anti-idiotypic antibodies, natural ligands of the receptor and anti-receptor antibodies2. Using agents which mimic the cellular receptor and bind to the VAP. This includes anti-VAP antibodies, receptor anti-idiotypic antibodies, extraneous receptor and synthetic receptor mimics.
This strategy of designing drugs can be very expensive, and since the process of generating anti-idiotypic antibodies is partly trial and error, it can be a relatively slow process until an adequate molecule is produced.
A very early stage of viral infection is viral entry, when the virus attaches to and enters the host cell. A number of "entry-inhibiting" or "entry-blocking" drugs are being developed to fight HIV.. Attempts to interfere with the binding of HIV with the CD4 receptor have failed to stop HIV from infecting helper T cells, but research continues on trying to interfere with the binding of HIV to the CCR5 receptor in hopes that it will be more effective.
However, two entry-blockers, amantadine and rimantadine, have been introduced to combat influenza, and researchers are working on entry-inhibiting drugs to combat hepatitis B and C virus.
One entry-blocker is pleconaril. Pleconaril works against rhinoviruses, which cause the common cold, by blocking a pocket on the surface of the virus that controls the uncoating process. This pocket is similar in most strains of rhinoviruses and enteroviruses, which can cause diarrhea, meningitis, conjunctivitis, and encephalitis.
During viral synthesis
A second approach is to target the processes that synthesize virus components after a virus invades a cell. One way of doing this is to develop nucleotide or nucleoside analogues that look like the building blocks of RNA or DNA, but deactivate the enzymes that synthesize the RNA or DNA once the analogue is incorporated.
The first successful antiviral, acyclovir, is a nucleoside analogue, and is effective against herpesvirus infections. The first antiviral drug to be approved for treating HIV, zidovudine (AZT), is also a nucleoside analogue.
An improved knowledge of the action of reverse transcriptase has led to better nucleoside analogues to treat HIV infections. One of these drugs, lamivudine, has been approved to treat hepatitis B, which uses reverse transcriptase as part of its replication process. Researchers have gone further and developed inhibitors that do not look like nucleosides, but can still block reverse transcriptase.
Other targets being considered for HIV antivirals include RNase H - which is a component of reverse transcriptase that splits the synthesized DNA from the original viral RNA - and integrase, which splices the synthesized DNA into the host cell genome.
Once a virus genome becomes operational in a host cell, it then generates messenger RNA (mRNA) molecules that direct the synthesis of viral proteins. Production of mRNA is initiated by proteins known as transcription factors. Several antivirals are now being designed to block attachment of transcription factors to viral DNA.
Genomics has not only helped find targets for many antivirals, it has provided the basis for an entirely new type of drug, based on "antisense" molecules. These are segments of DNA or RNA that are designed as "mirror images" to critical sections of viral genomes, and the binding of these antisense segments to these target sections blocks the operation of those genomes. A phosphorothioate antisense drug named fomivirsen has been introduced, used to treat opportunistic eye infections in AIDS patients caused by cytomegalovirus, and other antisense antivirals are in development. An antisense structural type that has proven especially valuable in research is morpholino antisense. 
Yet another antiviral technique inspired by genomics is a set of drugs based on ribozymes, which are enzymes that will cut apart viral RNA or DNA at selected sites. In their natural course, ribozymes are used as part of the viral manufacturing sequence, but these synthetic ribozymes are designed to cut RNA and DNA at sites that will disable them.
A ribozyme antiviral to deal with hepatitis C is in field testing, and ribozyme antivirals are being developed to deal with HIV. An interesting variation of this idea is the use of genetically modified cells that can produce custom-tailored ribozymes. This is part of a broader effort to create genetically modified cells that can be injected into a host to attack pathogens by generating specialized proteins that block viral replication at various phases of the viral life cycle.
Some viruses include an enzyme known as a protease that cuts viral protein chains apart so they can be assembled into their final configuration. HIV includes a protease, and so considerable research has been performed to find "protease inhibitors" to attack HIV at that phase of its life cycle. Protease inhibitors became available in the 1990s and have proven effective, though they can have unusual side effects, for example causing fat to build up in unusual places. Improved protease inhibitors are now in development.
Release phase
The final stage in the life cycle of a virus is the release of completed viruses from the host cell, and this step has also been targeted by antiviral drug developers. Two drugs named zanamivir (Relenza) and oseltamivir (Tamiflu) that have been recently introduced to treat influenza prevent the release of viral particles by blocking a molecule named neuraminidase that is found on the surface of flu viruses, and also seems to be constant across a wide range of flu strains.

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36  + 9 =     
austin invisalign braces  |  24-Sep-2010 18:38:09 IST
Yeah, Prodrug have some advantages over natural and traditional drugs.But it is not now used in massive phase.One day will come everyone will adopted with this type of drug.
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